Evidence map›Paper›PMID 25811933›Full record

ArticleGenes and immunity2015

Evidence that MHC I-E dampens thyroid autoantibodies and prevents spreading to a second thyroid autoantigen in I-A(k) NOD mice.

A-N Pelletier, H A Aliesky, B Banuelos, G Chabot-Roy, B Rapoport, S Lesage, S M McLachlan

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. The NOD Mouse Beyond Autoimmune Diabetes.Frontiers in immunology · 2022
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

A-N Pelletier1] Department of Immunology-Oncology, Maisonneuve-Rosemont Hospital, Montréal, QC, Canada [2] Département de Microbiologie, Infectiologie et Immunologie, Université de Montréal, Montréal, QC, Canada.
H A AlieskyThyroid Autoimmune Disease Unit, Cedars-Sinai Research Institute and UCLA School of Medicine, University of California, Los Angeles, CA, USA.
B BanuelosThyroid Autoimmune Disease Unit, Cedars-Sinai Research Institute and UCLA School of Medicine, University of California, Los Angeles, CA, USA.
G Chabot-RoyDepartment of Immunology-Oncology, Maisonneuve-Rosemont Hospital, Montréal, QC, Canada.
B RapoportThyroid Autoimmune Disease Unit, Cedars-Sinai Research Institute and UCLA School of Medicine, University of California, Los Angeles, CA, USA.
S Lesage1] Department of Immunology-Oncology, Maisonneuve-Rosemont Hospital, Montréal, QC, Canada [2] Département de Microbiologie, Infectiologie et Immunologie, Université de Montréal, Montréal, QC, Canada.
S M McLachlanThyroid Autoimmune Disease Unit, Cedars-Sinai Research Institute and UCLA School of Medicine, University of California, Los Angeles, CA, USA.
Cedars-Sinai Medical Center · USHôpital Maisonneuve-Rosemont · CAUniversity of California, Los Angeles · USUniversité de Montréal · CA

Funding

MODULATION OF AN ANIMAL MODEL OF HYPERTHYROIDISMR01DK054684 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI MCLACHLAN, SANDRA M · 1999 to 2017
$5.6M
GENETIC SUSCEPTIBILITY TO GRAVES'-LIKE HYPERTHYROIDISM IN MICER01DK082390 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI MCLACHLAN, SANDRA M · 2010 to 2014
$1.8M
NIDDK NIH HHS DK 082390NIDDK NIH HHS DK 54684NIDDK NIH HHS R01 DK054684NIDDK NIH HHS R01 DK082390
6 · The paper itself

Abstract

NOD.H2(k) and NOD.H2(h4) mice carry the major histocompatibility complex (MHC) class II molecule I-A(k) associated with susceptibility to experimentally induced thyroiditis. Dietary iodine-enhanced spontaneous thyroid autoimmunity, well known in NOD.H2(h4) mice, has not been investigated in NOD.H2(k) mice. We compared NOD.H2(h4) and NOD.H2(k) strains for thyroiditis and autoantibodies to thyroglobulin (TgAb) and thyroid peroxidase (TPOAb) without or with dietary sodium iodide (NaI) for up to 32 weeks. TgAb levels were significantly higher in NOD.H2(h4) compared with NOD.H2(k) mice on NaI, and TPOAb developed in NOD.H2(h4) mice but not in NOD.H2(k) mice. DNA exome analysis revealed, in addition to the differences in the chromosome (Chr) 17 MHC regions, that NOD.H2(k) mice, and particularly NOD.H2(h4) mice, have substantial non-MHC parental DNA. KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analysis highlighted thyroid autoimmunity and immune-response genes on Chr 17 but not on Chr 7, and 15 parental B10.A4R DNA. Studies of parental strains provided no evidence for non-MHC gene contributions. The exon 10 Tg haplotype, associated with experimentally induced thyroiditis, is absent in NOD.H2(h4) and NOD.H2(k) mice and is not a marker for spontaneous murine thyroid autoimmunity. In conclusion, the absence of I-E is a likely explanation for the difference between NOD.H2(h4) and NOD.H2(k) mice in TgAb levels and, as in humans, autoantibody spreading to TPO.

Indexed as

AnimalsAutoantibodiesAutoimmunityExomeHaplotypesHistocompatibility Antigens Class IIIodide PeroxidaseMaleMice, Inbred NODSodium IodideThyroglobulinThyroid GlandThyroiditisThyroiditis, AutoimmuneAutoantibodiesHistocompatibility Antigens Class III-E-antigenIodide PeroxidaseSodium IodideThyroglobulin

Identifiers

PMID25811933
PMCPMC4457582
OpenAlexW2053219172

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.